A mechano-electro-acoustical model for the cochlea: Response to acoustic stimuli

Ramamoorthy, Sripriya; Deo, Niranjan; Grosh, Karl

doi:10.1121/1.2713725

Cited by 138 publications

(192 citation statements)

References 46 publications

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“…Phase inconsistency between our results and others' likely resulted from differences in phase detection techniques, animal species, and measurement locations. Whereas the proposed cochlear micromechanical mechanism is well supported by experimental data, it does not exclude other mechanisms (33,(39)(40)(41)(42)(43)(44)(45)(46)(47)(48)(49).…”

Section: Discussionmentioning

confidence: 56%

Reticular lamina and basilar membrane vibrations in living mouse cochleae

Ren¹,

He²,

Kemp

2016

Proc. Natl. Acad. Sci. U.S.A.

121

134

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It is commonly believed that the exceptional sensitivity of mammalian hearing depends on outer hair cells which generate forces for amplifying sound-induced basilar membrane vibrations, yet how cellular forces amplify vibrations is poorly understood. In this study, by measuring subnanometer vibrations directly from the reticular lamina at the apical ends of outer hair cells and from the basilar membrane using a custom-built heterodyne low-coherence interferometer, we demonstrate in living mouse cochleae that the soundinduced reticular lamina vibration is substantially larger than the basilar membrane vibration not only at the best frequency but surprisingly also at low frequencies. The phase relation of reticular lamina to basilar membrane vibration changes with frequency by up to 180 degrees from ∼135 degrees at low frequencies to ∼-45 degrees at the best frequency. The magnitude and phase differences between reticular lamina and basilar membrane vibrations are absent in postmortem cochleae. These results indicate that outer hair cells do not amplify the basilar membrane vibration directly through a local feedback as commonly expected; instead, they actively vibrate the reticular lamina over a broad frequency range. The outer hair cell-driven reticular lamina vibration collaboratively interacts with the basilar membrane traveling wave primarily through the cochlear fluid, which boosts peak responses at the best-frequency location and consequently enhances hearing sensitivity and frequency selectivity.cochlea | outer hair cells | hearing | cochlear amplifier | interferometry A s the auditory sensory organ, the mammalian cochlea is able to detect soft sounds at levels as low as ∼20 μPa, equivalent to eardrum vibrations of <1-pm displacement (1), which is >100-fold smaller than the diameter of a hydrogen atom. The cochlea's remarkable sensitivity is commonly attributed to a micromechanical feedback system, which amplifies soft sounds using forces generated by outer hair cells (2-10). In addition to active bundle movements (2), mammalian outer hair cells are capable of changing their lengths in response to electrical stimulation in vitro (11)(12)(13)(14). This electromechanical force production is termed outer hair cell electromotility or somatic motility, which is produced by the membrane protein, prestin (15). Transgenic mice without prestin or with altered prestin suffer from severe hearing loss (4, 16). Targeted inactivation of prestin over well-defined cochlear segments dramatically reduces the traveling wave's peak response (17). Recent micromechanical measurements in sensitive living mouse cochleae showed (18) that electrical stimulation of outer hair cells induces vigorous vibrations of the reticular lamina at the apical surfaces of the outer hair cells. Whereas this experiment demonstrates that outer hair cells are capable of generating substantial forces to vibrate cochlear microstructures in vivo, the lack of frequency selectivity of the electrically induced reticular lamina vibration, however, is incons...

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Section: Discussionmentioning

confidence: 56%

Reticular lamina and basilar membrane vibrations in living mouse cochleae

Ren¹,

He²,

Kemp

2016

Proc. Natl. Acad. Sci. U.S.A.

121

134

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“…The attenuation of 6 dB/decade is a quite conservative estimate, because the BM wave envelopes used as the input for the calculation of the frequency dependence of the potentials were all normalised to the same peak amplitude. However, there may be significant boosting of the BM amplitudes towards the cochlear base: as much as a 30 dB increase is predicted for some cochlear models (Ramamoorthy et al 2007). This would provide a further 'flattening' of the OHC gain function.…”

Section: A Computational Laboratory For Studying Connexin Mutationsmentioning

confidence: 99%

Reduced Electromotility of Outer Hair Cells Associated with Connexin-Related Forms of Deafness: An In silico Study of a Cochlear Network Mechanism

Mistrík¹,

Ashmore²

2010

JARO

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Mutations in the GJB2 gene encoding for the connexin 26 (Cx26) protein are the most common source of nonsyndromic forms of deafness. Cx26 is a building block of gap junctions (GJs) which establish electrical connectivity in distinct cochlear compartments by allowing intercellular ionic (and metabolic) exchange. Animal models of the Cx26 deficiency in the organ of Corti seem to suggest that the hearing loss and the degeneration of outer hair cells (OHCs) and inner hair cells is due to failed K + and metabolite homeostasis. However, OHCs can develop normally in some mutants, suggesting that the hair cells death is not the universal mechanism. In search for alternatives, we have developed an in silico large scale three-dimensional model of electrical current flow in the cochlea in the small signal, linearised, regime. The effect of mutations was analysed by varying the magnitude of resistive components representing the GJ network in the organ of Corti. The simulations indeed show that reduced GJ conductivity increases the attenuation of the OHC transmembrane potential at frequencies above 5 kHz from 6.1 dB/decade in the wild-type to 14.2 dB/decade. As a consequence of increased GJ electrical filtering, the OHC transmembrane potential is reduced by up to 35 dB at frequencies 910 kHz. OHC electromotility, driven by this potential, is crucial for sound amplification, cochlear sensitivity and frequency selectivity. Therefore, we conclude that reduced OHC electromotility may represent an additional mechanism underlying deafness in the presence of Cx26 mutations and may explain lowered OHC functionality in particular reported Cx26 mutants.

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“…Note that in this respect, the OHC models of [9] and [4] are identical, although they are expressed quite differently. Using the vector x n = (ξ r , ξ r ,ξ o , ξ o ) T to represent the state of the nth micromechanical segment, these equations can be expressed in matrix state-space form asẋ where A n , B n and H n are respectively 5×5, 5×1 and 5×1 matrices.…”

Section: Mechanicalmentioning

confidence: 94%

“…In order to allow for the possibility of longitudinal electrical coupling, we adopt a model similar to that of [6,9,12], as shown in Fig. 1B.…”

Section: Mechanicalmentioning

confidence: 99%

An Electromechanical Model for the Cochlear Microphonic

Teal¹,

Lineton²,

Elliott³

et al. 2011

AIP Conference Proceedings

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Abstract. The first of the many electrical signals generated in the ear, nerves and brain as a response to a sound incident on the ear is the cochlear microphonic (CM). The CM is generated by the hair cells of the cochlea, primarily the outer hairs cells. The potentials of this signal are a nonlinear filtered version of the acoustic pressure at the tympanic membrane. The CM signal has been used very little in recent years for clinical audiology and audiological research. This is because of uncertainty in interpreting the CM signal as a diagnostic measure, and also because of the difficulty of obtaining the signal, which has usually required the use of a transtympanic electrode. There are however, several potential clinical and research applications for acquisition of the CM. To promote understanding of the CM, and potential clinical application, a model is presented which can account for the generation of the cochlear microphonic signal. The model incorporates micromechanical and macro-mechanical aspects of previously published models of the basilar membrane and reticular lamina, as well as cochlear fluid mechanics, piezoelectric activity and capacitance of the outer hair cells. It also models the electrical coupling of signals along the scalae.

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A mechano-electro-acoustical model for the cochlea: Response to acoustic stimuli

Cited by 138 publications

References 46 publications

Reticular lamina and basilar membrane vibrations in living mouse cochleae

Reticular lamina and basilar membrane vibrations in living mouse cochleae

Reduced Electromotility of Outer Hair Cells Associated with Connexin-Related Forms of Deafness: An In silico Study of a Cochlear Network Mechanism

An Electromechanical Model for the Cochlear Microphonic

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